Abstract
The cholinergic nervous system can inhibit the systemic inflammation accompanying sepsis by virtue of a specific action of acetylcholine on α7 cholinergic receptors. The current authors sought to determine the effect of nicotine, an α7 cholinergic receptor agonist, on the host response to pneumonia caused by Streptococcus pneumoniae.
Mice were intranasally infected with S. pneumoniae and treated with nicotine or saline intraperitoneally using a treatment schedule shown to improve host defence against abdominal sepsis.
Nicotine treatment was associated with a transiently enhanced growth of S. pneumoniae, as indicated by higher bacterial loads in both lungs and blood at 24 h after infection. At 48 h after infection, bacterial burdens had increased in both treatment groups and differences were no longer present. Remarkably, mice treated with nicotine showed enhanced lung inflammation at 24 h after infection. Moreover, both lung and plasma concentrations of the pro-inflammatory cytokines tumour necrosis factor-α and interferon-γ were higher in nicotine-treated animals at this time-point. Additional studies examining the effect of nicotine on the immediate (4-h) inflammatory response to S. pneumoniae did not reveal an anti-inflammatory effect of nicotine either.
The present data suggest that nicotine transiently impairs host defence in pneumococcal pneumonia.
Footnotes
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